Date on Master's Thesis/Doctoral Dissertation

5-2020

Document Type

Master's Thesis

Degree Name

M.S.

Department

Oral Biology

Degree Program

Oral Biology, MS

Committee Chair

Scott, David

Committee Co-Chair (if applicable)

Pisano, Michele

Committee Member

Pisano, Michele

Committee Member

Uriarte, Silvia

Author's Keywords

Cytokines; smoking; periodontitis; alveolar bone loss; p. gingivalis; mice

Abstract

Background: Tobacco smoking is the leading environmental risk factor for periodontal diseases. Delineation of the mechanisms underlying tobacco-induced or exacerbated periodontitis is hampered by the lack of an appropriate and reliable animal model. Hypothesis: We hypothesized that Porphyromonas-gingivalis-infected, cigarette smoke-exposed mice would represent reproducible models of acute (ligature model) and chronic (oral gavage model) tobacco-enhanced periodontitis that reflect multiple aspects of the disease noted in human smokers. Methods: In a chronic oral gavage disease model, Balb/c mice (6-8 weeks, 4 groups of n = 6 per group) were exposed to smoke produced by a Teague-10 smoking machine from 1R6F research cigarettes (20 cigarettes per day over 3 hours; mean carbon monoxide (CO), 150 ppm; mean particulate exposure, 4.9 mg/m3) or exposed to ambient air, over 68 days. The mice were repeatedly orally inoculated with Streptococcus gordonii and Porphyromonas gingivalis or sham inoculated. At euthanasia, the IgM and IgG response to infection; systemic inflammatory mediators; specific local gingival inflammatory indices (IL-1β, MMP-8, MMP-9, CD14and CD45); as well as alveolar bone loss were assessed. In an acute ligature-induced disease model, Balb/c mice (6-8 weeks, 4 groups of n = 7 per group) were exposed to smoke (20 cigarettes per day over 3 hours; mean CO, 200 ppm; mean particulate exposure, 9.8 mg/m3) or exposed to ambient air, over 14 days. The mice vii were repeatedly orally inoculated with P. gingivalis or sham inoculated. At euthanasia, IgM and IgG response to infection, alveolar bone loss was assessed. Plans to assess local and systemic inflammatory indices were curtailed by the Covid-19 outbreak. Results: In a chronic model of periodontitis, tobacco smoke exposure enhanced bacteria-induced bone loss (p< 0.01). Systemic innate immune suppression was also apparent, as indicated by reduced levels of systemic CCL2, CXCL1, MIP-1b,GM-CSF,IL-13, and IL-10 (all p< 0.05), while local expression of MMP-8 was augmented in infected mice (p< 0.05). However, tobacco smoke exposure did not influence murine mass, IgM or IgG ,or the mRNA signal of inflammatory mediator’s in murine gingiva. In the acute model of periodontitis, tobacco smoke exposure, again, enhanced bacteria-induced bone loss (p< 0.01). Body mass differentials were also influenced by smoke exposure (p

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